期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/ijms23084186
关键词
rat atrial myocardium; pulmonary hypertension; heart failure; isometric force-length relationship; slow force response; post-rest potentiation
资金
- Russian Science Foundation [21-15-00169]
- Russian Science Foundation [21-15-00169] Funding Source: Russian Science Foundation
There is a lack of data about the contractile behavior of the right atrial myocardium in chronic pulmonary heart disease. In this study, we found noticeable differences in the contractility and Ca transient of isolated right atrial strips between healthy rats and rats with monocrotaline-induced pulmonary hypertension, suggesting a potential compensatory effect of atrial myocardium in systolic deficiency.
There is a lack of data about the contractile behavior of the right atrial myocardium in chronic pulmonary heart disease. We thoroughly characterized the contractility and Ca transient of isolated right atrial strips of healthy rats (CONT) and rats with the experimental model of monocrotaline-induced pulmonary hypertension (MCT) in steady state at different preloads (isometric force-length), during slow force response to stretch (SFR), and during post-rest potentiation after a period of absence of electrical stimulation (PRP). The preload-dependent changes in the isometric twitch and Ca transient did not differ between CONT and MCT rats while the kinetics of the twitch and Ca transient were noticeably slowed down in the MCT rats. The magnitude of SFR was significantly elevated in the MCT right atrial strips and this was accompanied by the significantly higher elevation of the Ca transient relative amplitude at the end of SFR. The slow changes in the contractility and Ca transient in the PRP protocol did not differ between CONT and MCT. In conclusion, the alterations in the contractility and Ca transient of the right atrial myocardium of monocrotaline-treated rats with pulmonary hypertension mostly concern the elevation in SFR. We hypothesize that this positive inotropic effect in the atrial myocardium may (partly) compensate the systolic deficiency of the right ventricular failing myocardium.
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